Responses of serum inflammatory factor high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-alpha in elderly males with cerebral infarction Non-randomized concurrent control

BACKGROUND： Cerebral infarction is poorly treated due to neuronal necrosis and secondary pathophysiological changes; for example, free radical production and inflammatory reactions. OBJECTIVE： To detect the levels of high-sensitivity C-reactive protein （hs-CRP）, interleukin-6 （IL-6）, and tumor necrosis factor- a （TNF- α ） in elderly males with cerebral infarction. DESIGN： Non-randomized current control study. SETTING： Cadre Medical Department, Guizhou Provincial People＇s Hospital. PARTICIPANTS： Forty elderly males （65-89 years old） with cerebral infarction were selected from Cadre Medical Department, Guizhou Provincial People＇s Hospital from February 2004 to December 2006. All patients met the diagnostic criteria of cerebral infarction modified at the 4th National Cerebrovascular Disease Academic Meeting, and were diagnosed on the basis of CT or MRI tests. Furthermore, 35 elderly male inpatients （65-87 years old） without cerebral infarction were selected as the control group. Included subjects provided confirmed consent and did not have heart disease, diabetes mellitus, lipid disorder, acute trauma, infection, rheumatism, or other inflammatory diseases. The study was approved by the local ethics committee. There were no significant differences in age, blood pressure, and lipid levels between the cerebral infarction group and the control group （P 〉 0.05）, and this suggested that the baseline data of both groups were comparable. METHODS： Fasting venous blood was drawn from cerebral infarction patients 24 hours after cerebral infarction attack and from control subjects 24 hours after hospitalization. A latex-enhanced immunoturbidimetric assay and an enzyme-linked immunosorbent assay were used to detect the levels of hs-CRP, IL-6, and TNF- α in the serum. MAIN OUTCOME MEASURES： The levels of hs-CRP, 1L-6, and TNF- α in the serum in both groups. RESULTS： Forty cerebral infarction patients and thirty-five control subjects were included in the final analysis without any loss. Levels of hs-CRP, IL-6, and TNF-α in the cerebral infarction group were significantly higher than those in the control group （P 〈 0.01 ）. CONCLUSION： Levels of serum inflammatory reactive factors are increased in elderly males with cerebral infarction.

Serum Concentrations of Angiotensin, C-Reactive Protein, Interleukin-8, and Tumor Necrosis Factor-α in Train Driver Population

Train drivers are engaged in high-stress job. It may induce sleep, fatigue, and alertness loss at work, and endanger public safety. It’s unclear that cytokines of train driver would be influenced by their job. The research considers the hypothesis that stressful professions, such as train driver, influence the body’s immune system through the long-time and high-pressure working, and change production of neuro-immune factors. Using enzyme linked immunosorbent assay (ELISA), several neuro-immune factors were assayed among train drivers (N = 82) and health blood donors (N = 80) enrolled in the Yunnan Collaborative Innovation Center for Public Health and Disease Control. The concentrations of angiotensin, C-reactive protein (CRP), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) were determined. Kruskal-Wallis test and Dunn’s multiple comparisons test were performed for overall comparison between groups and for pairwise comparison, respectively. Statistical significance level was set at P < 0.05. The profession of train driving was not associated with significant increases or decreases in the systemic levels of inflammatory (CRP, IL-8, and TNF-α), but it was associated with the high expression of angiotensin in vivo. These findings suggest that the job of train driving may not be associated with significant alterations in systemic immune condition, but arouse the level of angiotensin.

Hepatitis B virus X protein up-regulates tumor necrosis factor-α expression in cultured mesangial cells via ERKs and NF-κB pathways

Objective:To investigate the effects of hepatitis B virus(HBV)X protein(HBx)on the expression of tumor necrosis factor-α(TNF-α)in glomerular mesangial cells(GMCs)and the underlying intracellular signal pathways.Methods:The plasmid pCI-neo-X that carries the X gene of hepatitis B virus was transfected into cultured GMCs.HBx expression in the transfected GMCs was assessed by Western-blot.TNF-αprotein and mRNA were assessed by ELISA and semi-quantitative RT-PCR,respectively.Three kinase inhibitors-U0126,an inhibitor of extracellular signal-regulated kinases(ERKs);lactacvstin,an inhibitor of nuclear factor-κB(NF-κB);and SB203580,a selective inhibitor of p38 MAP kinase(p38 MAPK)were used to determine which intracellular signal pathways may underlie the action of HBx on TNF-αexpression in transfected GMCs.Results:A significant increase in HBx expression in pCI-neo-X transfected GMCs was detected at 36 h and 48 h,which was not affected by any of those kinase inhibitors mentioned above.A similar increase in the expression of both TNF-αprotein and mRNA was also observed at 36 h and 48 h,which was significantly decreased in the presence of U0126 or lactacytin,but not SB203580.Conclusions:HBx upregulates TNF-αexpression in cultured GMCs,possibly through ERKs and NF-κB pathway,but not p38 MAPK pathway.

Helicobacter pylori tumor necrosis factor-α inducing protein promotes cytokine expression via nuclear factor-κB

AIM:To study the effects of Helicobacter pylori(H. pylori)tumor necrosis factor-α(TNF)inducing protein (Tip-α)on cytokine expression and its mechanism. METHODS:We cloned Tip-αfrom the H.pylori strain 26695,transformed Escherichia coli with an expression plasmid,and then confirmed the expression product by Western blotting.Using different concentrations of Tip-αthat affected SGC7901 and GES-1 cells at different times,we assessed cytokine levels using enzyme-linked immunosorbent assay.We blocked SGC7901 cells with pyrrolidine dithiocarbamate(PDTC),a specific inhibitor of nuclear factorκB(NF-κB).We then detected interleukin(IL)-1βand TNF-αlevels in SGC7901 cells. RESULTS:Western blot analysis using an anti-Tip-α antibody revealed a 23-kDa protein,which indicated that recombinant Tip-αprotein was recombined successfully.The levels of IL-1β,IL-8 and TNF-αwere sig-nificantly higher following Tip-αinterference,whether GES-1 cells or SGC-7901 cells were used(P<0.05).However,the levels of cytokines(including IL-1β,IL-8 and TNF-α)secreted by SGC-7901 cells were greater than those secreted by GES-1 cells following treatment with Tip-αat the same concentration and for the same duration(P<0.05).After blocking NF-κB with PDTC, the cells(GES-1 cells and SGC-7901 cells)underwent interference with Tip-α.We found that IL-1βand TNF-αlevels were significantly decreased compared to cells that only underwent Tip-αinterference(P<0.05). CONCLUSION:Tip-αplays an important role in cyto-kine expression through NF-κB.

Xuebijing alters tumor necrosis factor-alpha, interleukin-1beta and p38 mitogen activated protein kinase content in a rat model of cardiac arrest following cardiopulmonary resuscitation

We established a rat model of cardiac arrest by clamping the endotracheal tube of adult rats at expiration. Twenty-four hours after cardiopulmonary resuscitation, nerve cell injury and expression of tumor necrosis factor-α, interleukin-1β, and p38 mitogen activated protein kinase content were increased. Rats injected with Xuebijing, a Chinese herb compound preparation, exhibited normal cellular structure and morphology, dense neuronal cytoplasm, and decreased tumor necrosis factor-α, interleukin-1β, and p38 mitogen activated protein kinase expression at 24 hours following cardiopulmonary resuscitation. These data suggest that Xuebijing can attenuate neuronal injury induced by hypoxia and reperfusion during cardiopulmonary resuscitation.

Effect of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction in vivo

Acute myocardial infarction （AMI） is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-a （TNF-a） on ventricular arrhythmias induced byAMI in rats in vivo. Two hundred and forty male Wistar rats were randomized into a sham- operation group, an AMI group, and a recombinant human tumor necrosis factor receptor：Fc fusion protein（rhTNFR：Fc） group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery （LAD）, and there was no ligation but operation in the sham-operation group. The rhTNFR：Fc group was treated with rhTNFR：Fc（10 mg/kg）, a TNF-a antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-a among different groups were detected by histochemistry and real-time fluorescent quantitative PCR. Expression of TNF-a increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR：Fc group. The time- windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR：Fc group showed a lesser expression of TNF-a protein and a lower incidence of ventricular arrhythmias （P〈0.05）. There was no obvious change in the sham-operation group. The expression of TNF-a induced by AMI could contribute to the onset of ventricular arrhythmias.

Altered pattern of tumor necrosis factor-alpha production in peripheral blood monocytes from Crohn's disease

AIM To evaluate the inflammatory state in Crohn's disease(CD) patients and correlate it with genetic background and microbial spreading.METHODS By means of flow cytometry, production of tumor necrosis factor-alpha(TNF-α) was measured in peripheral blood monocytes from patients suffering from CD, ulcerative colitis(UC) and in healthy subjects after stimulation of the NOD2 and TLR pathways. CD patients were genotyped for the three most common NOD2 variants(R702W, G908 R and L1007Pfs*2) and basal production of TNF-α was correlated to NOD2 genotype. Also, production of TNF-α was correlated to plasmatic levels of LPS Binding Protein(LBP), soluble(s) CD14 and to the activity state of the disease.RESULTS The patients with CD were characterized by a significantly higher monocyte basal expression of TNF-αcompared with healthy subjects and UC patients, and after stimulation with Pam3CSK4(ligand of TLR2/1) and MDP-L18(ligand of NOD2) this difference was maintained, while other microbial stimuli(LPS, ligand of TLR4 and Poly I:C, ligand of TLR3) induced massive activation in CD monocytes as well as in UC and in healthy control cells. There was no significant difference in the production of TNF- α between patients who carried CD-associated heterozygous or homozygous variants in NOD2 and patients with wild type NOD2 genotype. Although serum LBP levels have been shown to correlate positively with the state of activity of the disease, TNF-α production did not show a clear correlation with either LBP or s CD14 levels in plasma. Moreover, no clear correlation was seen between TNF-α production and activity indices in either CD or UC.CONCLUSION Peripheral monocytes from CD express higher basal and stimulated TNF-α than controls, regardless of NOD2 genotype and without a clear correlation with disease activity.

Heat shock protein 70-2 and tumor necrosis factor-α gene polymorphisms in Chinese children with Henoch- Schönlein purpura

Background:Henoch-Schönlein purpura(HSP)or IgAassociated vasculitis is related to immune disturbances.Polymorphisms of the heat shock protein 70-2 gene(HSP70-2)and the tumor necrosis factor-αgene(TNF-α)are known to be associated with immune diseases.The purpose of this study was to investigate the likely association of HSP70-2(+1267A/G)and TNF-α(+308A/G)gene polymorphisms with HSP in children.Methods:The polymerase chain reaction restriction fragment length polymorphism method was used to detect the HSP70-2 and TNF-αpolymorphisms in 205 cases of children with HSP and 53 controls;and the association of these polymorphisms with HSP and HSP nephritis(HSPN)was analyzed.Results:The G/G genotypic frequencies at the+1267A/G position of HSP70-2 in the HSP group(22.9%)were signifi cantly higher than those in the healthy control group(9.4%)(χ^(2)=4.764,P<0.05).The frequencies of the A/A,A/G and G/G genotypes of HSP70-2 in patients in the nephritis-free group and the HSPN group showed no statistically significant difference.The A/A genotype frequency at the+308G/A position of TNF-αin the HSP group was 8.3%,which was higher than that in the control group(χ^(2)=6.447,P<0.05).The A allele frequency of TNF-αin the HSP group was higher than that in the control group,with a statistically significant difference(χ^(2)=7.241,P<0.05).Conclusions:The HSP70-2(+1267A/G)and TNF-α(+308G/A)gene polymorphisms were associated with HSP in children.The G/G homozygosity of HSP70-2 and the A/A homozygosity of TNF-αmay be genetic predisposing factors for HSP.

Effect of surfactant protein A on lipopolysaccharide-induced tumor necrosis factor-α expression in human proximal tubular epithelial cells

Background Surfactant protein A （SP-A） contributes to the regulation of sepsis-induced acute lung injury.In a previous study,we demonstrated the expression and localization of SP-A in the kidneys.The present study evaluated the effect of SP-A on lipopolysaccharide （LPS）-induced tumor necrosis factor-α （TNF-α） expression and its underlying mechanisms in the human renal tubular epithelial （HK-2） cells.Methods Indirect immunofiuorescence assay was used to detect SP-A distribution and expression in HK-2 cells.HK-2 cells were treated with various concentrations of LPS （0,0.1,1,2,5,and 10 mg/L） for 8 hours and with 5 mg/L LPS for different times （0,2,4,8,16,and 24 hours） to determine the effects of LPS on SP-A and TNF-α expression.Then,HK-2 cells were transfected with SP-A siRNA to analyze nuclear factor κB （NF-κB） P65 and TNF-α expression of HK-2 cells after LPS-treatment.Results Indirect immunofluorescence assay revealed that SP-A is localized to the membrane and cytoplasm of HK-2 cells.Interestingly,SP-A1/SP-A2 and TNF-α expression were found to be significantly increased in HK-2 cells upon LPS treatment.Transfection of LPS-treated HK-2 cells with SP-A siRNA resulted in significant increases in the levels of NF-κB P65 protein and TNF-α mRNA and protein compared to those in non-transfected LPS-treated HK-2 cells.Conclusion SP-A plays an important role in protecting cells against sepsis-induced acute kidney injury by inhibiting NF-κB activity to modulate LPS-induced increase in TNF-α expression.

Hepatitis B virus X protein upregulates tumor necrosis factor-α expression of rat mesangial cell line via ERKs pathway

Hepatitis B virus X protein(HBx),a 17-kd protein encoded by X gene of hepatitis B virus(HBV),has been shown to function as a transcriptional trans-activator of a variety of viral and cellular promoter/enhancer elements.The aim of the study is to investigate the extracellular regulated protein kinases(ERKs)pathway of HBx on glomerular mesangial cell(GMC)proliferation and tumor necrosis factor-α(TNF-α)expression.The HBV X gene was amplified by polymerase chain reaction(PCR),inserted into the eukaryotic expression vector pCI-neo and confirmed by restriction endonuclease digestion and sequence analysis.PCI-neo containing HBV X gene(pCI-neo-X)was then transfected into cultured GMC line via liposome.GMC proliferation,TNF-αand its mRNA expression were compared in the condition of with or without U0126 in culture media.HBx,ERK1/2 and p-ERK1/2 expression in GMCs was assessed by Western blotting.TNF-αmRNA expression was assessed by semi-quantitative reverse transcription-PCR(RT-PCR).TNF-αlevel in supernatants was measured by ELISA.GMC proliferation was detected by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide(MTT)kit.The results showed that HBx expression was found in transfected GMCs and became prominent at 36th and 48th h after transfection whether with or without U0126 in culture media.TNF-αmRNA expression was significantly decreased in U0126 group compared with U0126-free group.TNF-αlevels in supernatants in PCI-neo-X transfection without U0126 group were(189.0�18.1)and(172.3�24.3)pg/mL at 36th and 48th h after transfec-tion,respectively.In contrast,TNF-αlevels in supernatants with U0126 were(65.6�11.6)and(84.0�24.6)pg/mL at 36th and 48th h,respectively.The TNF-αlevels in the latter groups were significantly lower than those in the former groups(P<0.05).GMCs proliferation was also lower in added U0126 group at 36th and 48th h after transfection.From above,we can conclude that HBx could induce GMC proliferation and increase TNF-αmRNA expression and its protein production.HBx upregulates TNF-αexpression and induces cell proliferation of GMC line partly through ERK1/2 signal transduction pathway.

Fibrinogen-like protein 2 expression correlates with microthrombosis in rats with type 2 diabetic nephropathy

Fibrinogen-like protein 2 （fgl2）, a novel prothrombinase, is involved in microthrombosis. We examined fgl2 expression in the glomerular and tubulointerstitial capillaries and its correlation with microthromsis in rats with streptozocin-induced type 2 diabetic nephropathy. Our RT-PCR and immunoblotting analysis showed that fgl2 mRNA and protein levels were increased in microvascular endothelial cells of the glomeruli and renal interstitia at week 19 and became significantly elevated with the development of diabetic nephropathy （P 〈 0.01）. Fgl2 was not or only weakly expressed in the renal tissues of normal rats. Furthermore, a direct significant correlation （r = 0.543, P 〈 0.01） was found between fgl2 expression and microthrombotic capillaries in the renal tissues. Enzyme linked immunosorbent assays （ELISA） additionally showed that circulating TNF-α levels in rats with type 2 diabetes were significantly elevated and closely correlated with fgl2 expression （r = 0.871, P 〈 0.01）. Our results suggest that fgl2 may activate renal microthrombosis, thus contributing to glomerular hypertension and renal ischemia.

“Three Methods and Three Points” regulates p38 mitogen-activated protein kinase in the dorsal horn of the spinal cord in a rat model of sciatic nerve injury

Tuina is a traditional Chinese treatment for sensory disturbances caused by peripheral nerve injury and related diseases. Our previous studies showed that tuina regulates relevant regions and indices of the spinal dorsal horn using the Dian, Bo, and Rou method in Yinmen（BL37）, Yanglingquan（GB34）, and Weizhong（BL40）. Treatment prevents muscle atrophy, protects spinal cord neurons, and promotes sciatic nerve repair. The mechanisms of action of tuina for treating peripheral nerve injury remain poorly understood. This study established rat models of sciatic nerve injury using the crushing method. Rats received Chinese tuina in accordance with the principle of ＂Three Methods and Three Points,＂ once daily for 20 days. Tuina intervention reduced paw withdrawal latency and improved wet weight of the gastrocnemius muscle, as well as promoting morphological recovery of sciatic nerve fibers, Schwann cells, and axons. The protein expression levels of phospho-p38 mitogen-activated protein kinase, tumor necrosis factor-α, and interleukin-1β also decreased. These findings indicate that ＂Three Methods and Three Points＂ promoted morphological recovery and improved behavior of rats with peripheral nerve injury.

Silencing the gene encoding C/EBP homologous protein lessens acute brain injury following ischemia/reperfusion

C/EBP homologous protein, an important transcription factor during endoplasmic reticulum stress, participates in cell apoptosis mediated by endoplasmic reticulum stress. Previous studies have shown that C/EBP homologous protein mediates nerve injury during Alzheimer＇s disease, subarachnoid hemorrhage and spinal cord trauma. In this study, we introduced C/EBP homologous protein short hairpin RNA into the brains of ischemia/reperfusion rat models via injection of lentiviral vector through the left lateral ventricle. Silencing C/EBP homologous protein gene expression significantly reduced cerebral infarction volume, decreased water content and tumor necrosis factor-α and interleukin-1β mRNA expression in brain tissues following infarction, diminished the number of TUNEL-positive cells in the infarct region, decreased caspase-3 protein content and increased Bcl-2 protein content. These results suggest that silencing C/EBP homologous protein lessens cell apoptosis and inflammatory reactions, thereby protecting nerves.

Effects of insulin aspart and metformin on gestational diabetes mellitus and inflammatory markers

BACKGROUND Gestational diabetes mellitus(GDM)refers to hyperglycemia caused by insulin resistance or insufficient insulin secretion during pregnancy.Patients with GDM have a high risk of pregnancy complications,which can adversely affect both maternal and fetal health.Therefore,early diagnosis,treatment and monitoring of GDM are essential.In recent years,a new treatment scheme represented by insulin aspart combined with metformin has received increasing attention.AIM To explore the effects of insulin aspart combined with metformin on patients with GDM and inflammatory markers.METHODS From April 2020 to September 2022,124 patients with GDM in Sanya Women and Children’s Hospital Managed by Shanghai Children’s Medical Center were collected and analyzed retrospectively.The control group(CG)comprised 62 patients treated with insulin aspart alone,and 62 patients treated with insulin aspart and metformin formed the observation group(OG).Before and after treatment,improvement of blood-glucose-related indexes[fasting blood glucose(FBG),2-h postprandial glucose(2h PG)and hemoglobin A1c(HbA1c)],serum related factor[serum homocysteine(Hcy)],serum inflammatory cytokines[tumor necrosis factor(TNF)-α,interleukin(IL)-6 and C-reactive protein(CRP)]were compared between the two groups.The clinical efficacy,adverse pregnancy outcomes and incidence of pregnancy complications were compared between the two groups.RESULTS After treatment,the levels of FBG,2h PG,HbA1c,Hcy,TNF-α,IL-6 and CRP in both groups were significantly decreased(P<0.05),and the levels of FBG,2h PG,HbA1c,Hcy,TNF-α,IL-6 and CRP in the OG were lower than in the CG(P<0.05).The total clinical effectiveness in the OG was higher than that in the CG(P<0.05).The total incidence of adverse pregnancy outcomes and complications in the OG was significantly lower than in the CG(P<0.05).CONCLUSION Insulin aspart combined with metformin are effective for treatment of GDM,which can reduce blood-glucoserelated indexes,Hcy and serum inflammatory cytokines,and risk of adverse pregnancy outcomes and complications.

L-and T-type Ca^(2+)channels dichotomously contribute to retinal ganglion cell injury in experimental glaucoma

Retinal ganglion cell apoptotic death is the main pathological characteristic of glaucoma,which is the leading cause of irreversible blindness.Disruption of Ca^(2+)homeostasis plays an important role in glaucoma.Voltage-gated Ca^(2+)channel blockers have been shown to improve vision in patients with glaucoma.However,whether and how voltage-gated Ca^(2+)channels are involved in retinal ganglion cell apoptotic death are largely unknown.In this study,we found that total Ca^(2+)current densities in retinal ganglion cells were reduced in a rat model of chronic ocular hypertension experimental glaucoma,as determined by whole-cell patch-clamp electrophysiological recordings.Further analysis showed that L-type Ca^(2+)currents were downregulated while T-type Ca^(2+)currents were upregulated at the later stage of glaucoma.Western blot assay and immunofluorescence experiments confirmed that expression of the Ca_(V)1.2 subunit of L-type Ca^(2+)channels was reduced and expression of the Ca_(V)3.3 subunit of T-type Ca^(2+)channels was increased in retinas of the chronic ocular hypertension model.Soluble tumor necrosis factor-α,an important inflammatory factor,inhibited the L-type Ca^(2+)current of isolated retinal ganglion cells from control rats and enhanced the T-type Ca^(2+)current.These changes were blocked by the tumor necrosis factor-αinhibitor XPro1595,indicating that both types of Ca^(2+)currents may be mediated by soluble tumor necrosis factor-α.The intracellular mitogen-activated protein kinase/extracellular signal-regulated kinase pathway and nuclear factor kappa-B signaling pathway mediate the effects of tumor necrosis factor-α.TUNEL assays revealed that mibefradil,a T-type calcium channel blocker,reduced the number of apoptotic retinal ganglion cells in the rat model of chronic ocular hypertension.These results suggest that T-type Ca^(2+)channels are involved in disrupted Ca^(2+)homeostasis and apoptosis of retinal ganglion cells in glaucoma,and application of T-type Ca^(2+)channel blockers,especially a specific CaV3.3 blocker,may be a potential strategy for the treatment of glaucoma.

慢性阻塞性肺疾病急性加重期血清瘦素与肺功能关系的临床研究

目的：探讨血清瘦素（ leptin ）与慢性阻塞性肺疾病（ chronic obstructive pulmonary disease， COPD）急性加重期患者肺功能的关系。方法选择COPD急性加重期患者35例、COPD稳定期患者38例及健康志愿者30例，抽取空腹血。用放免法测定血清瘦素、用酶联免疫吸附法（ELISA）测定肿瘤坏死因子-α（TNF-α）及用全自动生化仪检测C-反应蛋白（CRP）；检测肺功能，记录1 s用力呼气量（ FEVl ）、最大通气量（ MVV）、肺一氧化碳弥散量（ DLCO ）等指标、分析COPD急性加重期患者血清瘦素水平与TNF-α、CRP、肺功能等的相关性。结果①COPD急性加重期患者血清瘦素、TNF-α、CRP均明显高于COPD稳定期组和对照组，而FEVl、MVV、DLCO则明显低于后者；②COPD急性加重期患者血清瘦素与TNF-α、CRP呈正相关，与FEVl、MVV、DLCO呈负相关。结论血清瘦素可判断COPD急性加重期预后，可以评估肺功能损害风险。

二甲双胍对2型糖尿病患者血浆ET-1和血清hs-CRP、TNF2水平的影响

目的探讨了二甲双胍对DM2T2DM患者血浆ET-1和血清HS-CRP、TNF2水平的影响。方法应用放射免疫分析法和免疫比浊法对33例T2DM患者进行了血浆ET-1和血清HS-CRP、TNF2水平检测,并与35名正常健康人做比较。结果 T2DM患者在治疗前血浆ET-1和血清HS-CRP.TNF2水平均非常显著地高于正常人组(P<0.01)经二甲双胍治疗了3个月后,血浆ET-1和血清HS-CRP、TNF2水平与正常人比较无显著性差异(P>0.05)且ET-1水平与HS-CRP、TNF2水平成正相关(R=0.618 4、0.594 8 P<0.01)。结论二甲双胍具有改善血管内皮功能的作用。

Changes of Src-suppressed C kinase substrate expression in cytokine induced reactive C6 glioma cells

Objective To investigate effect of tumor necrosis factor-or （TNF-α） on the Src-suppressed C kinase substrate （SSeCKS） in C6 glioma cells. Methods Cultured C6 glioma cells were randomly divided into two groups. In time-dependent group, cells were cultured with TNF-α （2 ng/mL） for 0 h, 1 h, 3 h, 6 h, 12 or 24 h, respectively; in dose-dependent group, cells were cultured with TNF-α （0 ng/mL, 0.02 ng/mL, 0.2 ng/mL, or 2 ng/mL） for 6 h. The expression of SSeCKS was detected by Realtime PCR and Western blot analysis, and immunocytochemistry was used to investigate SSeCKS＇s subcellular localization. Results TNF-α induced rapid phosphorylations of protein kinase C （PKC） substrates in C6 glioma cells, and upregulated SSeCKS expression in a time and concentration dependent manner. Immunocytochemistry suggested that SSeCKS was localized in the cyroplasm and the leading end of podosomal extensions in control groups, while TNF-α induced translocation of SSeCKS perinuclear. This effect could be partly reversed by PKC inhibitor Ro-31-8220. Conclusion TNF-α activates PKC and upregulates SSeCKS expression in C6 glioma cells. These effects are associated with PKC activity, suggesting that SSeCKS plays a role in response to glia activation in PKC mediated pathway.

Adaptive and regulatory mechanisms in aged rats with postoperative cognitive dysfunction

Inflammation may play a role in postoperative cognitive dysfunction. 5＇ Adenosine monophos- phate-activated protein kinase, nuclear factor-kappa B, interleukin-1β, and tumor necrosis factor-a are involved in inflammation. Therefore, these inflammatory mediators may be involved in postoperative cognitive dysfunction. Western immunoblot analysis revealed 5＇ adenosine mo- nophosphate-activated protein kinase and nuclear factor-kappa B in the hippocampus of aged rats were increased 1-7 days after splenectomy. Moreover, interleukin-1β and tumor necrosis fac- tor-α were upregulated and gradually decreased. Therefore, these inflammatory mediators may participate in the splenectomy model of postoperative cognitive dysfunction in aged rats.

Effects of wind-dispelling drugs and deficiency-nourishing drugs of Houshiheisan compound prescription on astrocyte activation and inflammatory factor expression in the corpus striatum of cerebral ischemia rats

This study explored protective effects of Houshiheisan and its compound prescription of wind-dispelling drugs and deficiency-nourishing drugs on cerebral ischemia in terms of astrocyte activation and inflammatory factor expression.Results suggested that Houshiheisan lessened neuronal degeneration in the corpus striatum on the ischemic side of rats following cerebral ischemia/reperfusion injury,contributed to astrocyte activation and glial fibrillary acidic protein expression in the corpus striatum and decreased the levels of interleukin-2,interleukin-6, interleukin-1βand tumor necrosis factor-α.Factor analysis results demonstrated that deficiency-nourishing drugs were more beneficial in protecting neurons and upregulating glial fibrillary acidic protein expression than wind-dispelling drugs.However,wind-dispelling drugs were more effective in increasing the number of glial fibrillary acidic protein-positive cells and reducing inflammatory factor expression than deficiency-nourishing drugs.These indicate that different ingredients of Houshiheisan suppress cerebral ischemic injury by promoting astrocyte activation and diminishing inflammatory factor expression.